P3 TP III jones immunopath

boosts immune system

:)

defense mechs before infection



-mechs stimulated by microbes and antigens

Cell mediated- defense against intracelluar microbes

Humoral Mediated- defense against extracellualar microbes and toxins (bacteria)

- thymus derived

CD4+ T cells- surface antigen binders, bind MHC II

CD8 T cells- cytotoxic T cells, bind MHC I antigen

mediate humoral immunity

become plasma cells and secrete antibody

IgG, IgM, IgE, IgA

IgM- first antibodies on site (new infection)

IgG- old infection (fast rechallenge)

IgA- in places open to environmental areas

- presents antigen

D-- present antigen to CD4 cells, have BOTH HLA I and II (thats special)

nk- lyse cells that dont look good
can lyse IgG coated target cells - Antibody dependant cell mediated cytoxicity ADCC

proteins modulate function other cell types

interleukins ILs- act mostly on leukocytes (IL2, 4 act on lymphocyte active,growth,development)

TNF-a, TNF-b, IFN-y, IL 5,10, 12 activate inflam

function bind peptide fragments of foreign proteins to show right T cells shits going down

on all nucleated cells and platelets---NOT IMMUNE cells...cept dendritic

bind stuff from inside cell like viral proteins, show on outside and wait for cytox T

alpha 1 and alpha2 domains

on immune cells

alpha 1 and beta 1 domains form the groove

recognized by CD4 helper T cells

anaphylactic

rapid, hyperesponsive after mast cells or basophils active in previously sensitized person

initial response- vasodilation nad vascular leakage occurs


late response- 2-8 hours later no further exposure, intense infiltration of tissues by phils

can cause tissue destruction, inflam

Rh blood type and shit

complement dependant rxn- rather direct lysis or opsonization (macrophage prep)

antibody dependant cell mediated cytoxicity- cell lysis w/o phagocytes

antibody mediated cellular dysfunction- stimulatory or inhibitory processes

ex myastenia gravis, graves disease

immune complex mediated

induced by antigen-antibody complexes

first formation of complexes in circulation

next deposit those in tissues

inflam rxn at sites across body

PPD? immune response to mycobacterium tuberculosis

involve CD4 and CD8, may be key player in transplant rejection

form granulomas, barrier keeps shit quarantined (cuz shit cant be killed i think)

death immature selfreactive T and B lymphos in thymus

escape negative selection,

deleted by anergy, suppressed by tcells or clonal deletion(apoptosis)

array of autoantibodies mostly antinuclear antibodies

activates help Ts and B cells

ANAs directed at nuclear antigens---DNA, histones, nucleolar antigens

false positive for syphilis, prolonged PTT

kidneys, joints, skin, RBCs suffer

dry eyes and dry mouth---fibrosis destruction lacrimal and salivary glands

2 ribonucleoprotein antigens SS-A, SS-B

failure B cells differentiate due to mutation Bruton tyrosine kinase

apparent at 6 months of age

defect in thymic development

T cell activation abscent

intrinsic B cell defects and abnormal T cells activation B cells

B cells cant mature to plasma cells

most common IDD

cant produce IgA cells....

most common X linked (yay)

defective IL-7

suseptable to...everything

defiency enzyme ADENOSINE DEAMINASE (ADA)

AIDS!

caused by HIV

Sexual transmission, mostly MSM in US

virus in semen and vagina and cervical cells

other STDs increase likeiness transmission

mother to infant is called vertical transmission

AIDs demetia can occur from cytokine responses, not from virus itself

Acute- 3-6 wks, sore throat, fever, rash, CD4 reduction but return to normal
viremia abates but virus replicates in specific cells

Chronic-lymphadenopathy develops, minor opportunistic infections
CD4 decline

Crisis- breakdown, viremia
fever for >1 month
CD4 lessthan 500

ELISA- 99%, p24 readily detectable

Western Blot- 2 bands from either gag or env region must be present for +ve

Viral Load-useful indicator of disease progess

deposition of proteinaceous substance tween cells of body

combo of diff diseases